eMedicine Specialties > Radiology > Genitourinary
Renal Artery Stenosis/Renovascular Hypertension: Imaging
Updated: Oct 2, 2009
Radiography
Findings
For the detection of RAS, hypertensive urography is obsolete.
Degree of Confidence
Hypertensive urography is of historical interest only. It is no longer used as a screening technique for RAS because of its inconsistent results. The urogram may be normal in the presence of established RAS.
Computed Tomography
Findings
The patient is a 39-year-old man with Leriche syndrome. The abdominal aorta is completely occluded just below the origin of the renal arteries. The right renal artery is completely occluded. Angioplasty and stenting of these arteries can be attempted via the brachial artery.
Image of a 39-year-old man with Leriche syndrome. The abdominal aorta is completely occluded just below the origin of the renal arteries. The right renal artery is completely occluded. Angioplasty and stenting of these arteries can be attempted via the brachial artery (same patient as in Image 14 in Multimedia).
Image of a 39-year-old man with Leriche syndrome. The abdominal aorta is completely occluded just below the origin of the renal arteries. The right renal artery is completely occluded. Angioplasty and stenting of these arteries can be attempted via the brachial artery (same patient as in Images 14-15 in Multimedia).
Image of a 39-year-old man with Leriche syndrome. The abdominal aorta is completely occluded just below the origin of the renal arteries. The right renal artery is completely occluded. Angioplasty and stenting of these arteries can be attempted via the brachial artery (same patient as in Images 14-16 in Multimedia).
Image of a 39-year-old man with Leriche syndrome. Note the atrophic right kidney and stenosis of the left renal artery with post-stenotic dilatation. The abdominal aorta is completely occluded just below the origin of the renal arteries. The right renal artery is completely occluded. Angioplasty and stenting of these arteries can be attempted via the brachial artery. Angioplasty and stenting of these arteries can be attempted via the brachial artery (same patient as in Images 14-17 in Multimedia).
CTA with MIP and quantitative measurement of stenosis is an accurate noninvasive technique in the diagnosis of RAS. The advent of spiral and multisection CT scanning has made CTA feasible. Continuous scanning through an area of interest during a single breath-hold provides sufficient data to reconstruct 3-dimensional (3D) images (see Images above and Images 14-18 in Multimedia).
Many scanning protocols are available. The general consensus is that both a timed bolus and rapid injection rate improve image quality. No positive oral contrast material should be used because it results in severe degradation of the image quality. Immediately before the procedure, the patient ingests water, and glucagon is then given intravenously to diminish bowel movement and maximize bowel distention. The 3 most common techniques used for 3D reconstruction are MIP, shaded-surface display (SSD), and volume rendering. MIP is often the single most useful technique for 3D reconstructions.
Accessory renal arteries are reliably identified by means of CTA. In either the mainstem artery or its intrarenal branches, RAS is detected with a high degree of accuracy.27,28,29,30
Degree of Confidence
The sensitivity and specificity of spiral CT in detecting RAS are approximately 98% and 94%, respectively. In patients with a plasma creatinine concentration higher than 1.7 mg/dL, the accuracy is lower (93% sensitivity, 81% specificity), possibly because of reduced renal blood flow. Because most of the false-negative and false-positive findings arise from accessory renal arteries, the accuracy in detecting RAS of the main renal artery may be as good as that of angiography.
False Positives/Negatives
Andreoni et al raised concerns that CTA or MRA may cause clinicians to overlook mild cases of digital subtraction angiography (DSA)-detectable AD.31 Most of the false-negative and false-positive findings of RAS are related to accessory renal arteries.
Magnetic Resonance Imaging
Findings
Renal artery stenosis/renovascular hypertension. Three-dimensional phase-contrast magnetic resonance angiographic (MRA) images of normal renal arteries.
Renal artery stenosis/renovascular hypertension. Dynamic gadolinium-enhanced magnetic resonance angiogram (MRA) shows normal renal arteries.
MRA is fast becoming a clinical standard for the safe and noninvasive detection of RAS, aneurysms, and occlusions. A comprehensive examination includes both 3D dynamic gadolinium-enhanced and 3D phase-contrast MRA techniques, which allow an evaluation of the renal arteries and other visceral arteries. The 3D phase-contrast technique is flow based and subject to dephasing in the presence of significant arterial stenosis. The 3D gadolinium-enhanced MRA method produces excellent contrast angiograms without the risk of iodinated compounds or radiation exposure (see Images above and Images 6-7 in Multimedia).
MRA provides accurate information about the number of renal arteries, the size of the kidneys, and the presence of anatomic variants.32,33,34
Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans.
As of late December 2006, the FDA had received reports of 90 such cases of NSF/NFD. Worldwide, over 200 cases have been reported, according to the FDA. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.
Degree of Confidence
Gadolinium-enhanced MRA has been proven to have high sensitivity for detecting stenosis in the main and accessory renal arteries. At presentation, MRA provides anatomic information regarding a vascular stenosis, but it provides little information about the functional significance of a stenosis. Studies have shown that 3D MRA with gadolinium-based contrast agents (which have a low potential for nephrotoxicity) has a sensitivity of 96-100% and a specificity of 71-96% for the detection of a main RAS of greater than 50%.
When combined with cardiac synchronization, 3D MRA can sharply delineate the entire length of the major renal arteries. However, MRA remains suboptimal for the detection of hemodynamically significant lesions of distal, intrarenal, and accessory renal arteries, which may cause physiologically significant RAS.
Limitations of MRA include its cost and lack of availability. Contraindications to MRA include claustrophobia and the presence of metallic implants, such as a pacemaker or surgical clip.
False Positives/Negatives
Andreoni et al raised concerns that CTA or MRA may cause clinicians to overlook mild cases of digital subtraction angiography (DSA)-detectable AD.31 Although false-negative studies in RAS are rare, a tendency to overestimate stenoses occurs, and this overestimation may lead to a false-positive diagnosis. To some extent, this tendency to overestimate stenoses can be compensated for by performing phase-contrast MRA, a type of MRA that utilizes accumulated phase differences.
Ultrasonography
Findings
Renal artery stenosis/renovascular hypertension. Left, Sonograms of the kidneys on a 57-year-old woman with difficult-to-control hypertension shows kidneys of uneven sizes: The left kidney is 96 mm, and the right kidney is 63 mm. Top right, Isotopic renogram (obtained with technetium mercaptoacetyltriglycine [MAG3]) after captopril shows a markedly depressed renal function in the right kidney. Bottom right, Analogous images show negligible activity in the right kidney. Note that this pattern is more typical for DTPA than MAG3 (as DTPA depends on the glomerular filtration rate for uptake which is decreased after captopril in renovascular hypertension [RVHT]). In severe cases of RVHT, MAG3 uptake can be decreased, as in this case. However, typically, uptake is preserved with decreased cortical excretion.
Renal artery stenosis/renovascular hypertension: Sonograms of the kidneys of a 46-year-old woman with difficult-to-control hypertension showing uneven sizes of the kidneys. The right kidney is 2.5 cm smaller in size. An isotope renogram obtained with technetium mercaptoacetyltriglycine (Tc-MAG3) shows renal function in the right kidney (purple) to be markedly depressed.
The diagnosis of RAS is made on the basis of systolic and diastolic velocity changes throughout the length of the renal artery (see Image above and Image 1 in Multimedia). Renal artery flow patterns can be classified into 4 categories: (1) normal, (2) diameter-reducing stenosis of less than 60%, (3) diameter-reducing stenosis of more than 60%, and (4) renal artery occlusion.
The peak systolic velocity in normal renal arteries averages 120 cm/s ±12, with an average peak systolic aortic velocity of 60 m/s ±15. Both velocities decrease with age.
The kidneys have a low-resistance vascular bed; thus, the Doppler spectral waveform from the normal kidney is that of a constant forward diastolic flow. In renal parenchymal disease, there is increased vascular resistance, which causes a decrease in the diastolic flow component and an increase in the pulsatility of the Doppler spectral waveform. Parenchymal diastolic flow velocities of less than 20% of the peak systolic velocities are consistent with renal parenchymal disease.
In RAS, the peak systolic velocity increases by more than 150 cm/s for angles less than 60° and by more than 180 cm/s for angles greater than 70°. Poststenotic spectral broadening may be present with or without flow reversal. Flow may be absent during diastole in a stenosis of more than 50%. A ratio of the peak systolic renal artery velocity to the aortic peak systolic velocity of 3.5 or more is said to be predictive of a stenosis of more than 60%.
Certain indirect Doppler sonographic signs have been described for RAS. One such sign is the presence of tardus-pavus pulse, which is demonstrated by a gradual slope of Doppler waveform during systole (pulse time increase of greater than 0.07-0.12 s) and an attenuation of Doppler waveform amplitude (peak systolic velocity less than 20-30 cm/s). The acceleration index is determined by dividing the slope of the systolic upstroke (in kilohertz per second) by the carrier Doppler frequency. The acceleration time is the interval between the onset of systole and the initial peak. The acceleration index in RAS is greater than 3 m/s2. The resistive index in RAS is usually less than 0.56. The early systolic peak may be absent in RAS.
Color-flow Doppler imaging may demonstrate disorganized flow patterns and a high velocity flow stream associated with hemodynamically significant stenosis. A false-negative diagnosis may occur with an accessory renal artery, whereas a false-positive diagnosis may be made with coarctation of the aorta.
In about 10% of patients who undergo renal transplantation, RAS occurs in the transplanted kidney. This raises the question of whether RAS is the cause of post-transplant hypertension. The site of stenosis is not an anastomotic site in most patients; this suggests the possibility of focal rejection (with edema/fibrosis) as the cause of the hypertension. Duplex and color-Doppler sonography have greatly affected the diagnosis of RAS. The most reliable Doppler criteria for stenosis are a high-velocity jet and distal turbulence.35
Degree of Confidence
Doppler sonography has several limitations in the diagnosis of RAS. These include patient-related factors, anatomic factors, technical factors, and pathologic factors.
Patient-related factors include bowel gas, obesity, respiratory renal movements, and poor patient compliance.
Anatomic factors include multiple renal arteries (16-28%), variation of renal veins (used as imaging landmarks), horseshoe kidneys, and crossed ectopia.
Technical factors include false-positive examination results associated with suboptimal angles, variation in operator experience, incomplete examination (because complete renal evaluation is cumbersome), the need to visualize the entire length of artery, transmitted cardiac and/or aortic pulsation (which may obscure renal waveforms), and different emphases on variable parameters.
Pathologic factors include false tracings (which may be recorded from large collateral vessels and a reconstituted main renal artery) and the presence of disorders that are associated with RAS and that affect different sites (eg, atheroma, fibromuscular hyperplasia, vasculitis, arteriovenous fistula, retroperitoneal fibrosis, neurofibromatosis).
False Positives/Negatives
A false-negative diagnosis may occur with accessory renal artery, whereas a false-positive diagnosis may be made with coarctation of the aorta.
Nuclear Imaging
Findings
Standard renography with iodine-131 (131 I)–labeled ortho-iodohippurate (OIH) is of historical interest and is no longer performed in the investigation of RAS.
The effect of the ACE inhibitor captopril on RAS was first described by Majd et al in 1983.36 They observed virtually no radionuclide uptake on diethylene triamine pentaacetic acid (DTPA) images in a patient with hypertension receiving captopril therapy. A repeat DTPA renogram performed in the same patient after cessation of captopril therapy revealed normal, bilateral DTPA uptake.
A number of mechanisms have been proposed to explain the effects Majd et al observed,36 although none explain the entire observed phenomenon. Normally, a balance maintains glomerular filtration in vascular tone between the preglomerular and postglomerular arterioles. With significant RAS, this balance is disturbed, because the pressure in the preglomerular arteriole is decreased and the filtration pressure can be maintained only by the postglomerular arteriolar vasoconstriction mediated by the renin-angiotensin system.
The administration of an ACE inhibitor such as captopril prevents the conversion of angiotensin I to the active vasoconstrictors angiotensin II and angiotensin III. By inhibiting the compensatory increase in vascular tone at the postglomerular arteriole, ACE inhibitors decrease glomerular filtration in the setting of RAS. The administration of ACE inhibitors in conjunction with radionuclide renography provides a noninvasive method for the detection of functionally significant RAS.37,38
Several radiopharmaceuticals with different clearance mechanisms are available, although all show a degree of clearance via glomerular filtration. In particular, DTPA is primarily cleared by means of glomerular filtration. The decreased clearance of DTPA induced by ACE inhibitors in RAS, as Majd et al observed, is readily shown on renograms as a decrease in function in the affected kidney and a deterioration in the renogram curve.36
In patients with RAS, effective renal plasma flow (ERPF) is shown to increase after the administration of an ACE inhibitor because of the efferent arteriolar vasodilatation, which increases blood flow through the renal parenchyma and decreases blood flow through the glomerulus.131 I-labeled OIH also closely estimates ERPF. Technetium (Tc)-labeled mercaptoacetyltriglycine (MAG3) has also been used to qualitatively assess ERPF (see Image below and Image 10 in Multimedia).
Renal artery stenosis/renovascular hypertension. Technetium mercaptoacetyltriglycine (Tc-MAG3) isotopic renogram in the same patient as in Images 8-9 in Multimediashows curves before and after angioplasty.
Since the introduction of captopril renography, various modifications have been made. Some centers use only 1 agent, either DTPA or MAG3. A positive result on ACE inhibition radionuclide scanning indicates that RVHT is present; it also implies the existence of hemodynamically significant RAS (>60-75% of the lumen).
It is important to understand that the criteria for interpreting a result as being positive depend upon the tracer used. If DTPA is used, there should be a change in split function if RVHT is present (since DTPA is dependent upon GFR for uptake, the initial uptake in the affected kidney will be decreased). If MAG3 is used, split function will usually not change, but there will be an increase in cortical retention (usually measured as 20 minute to maximum ratio) in the affected kidney. This is because initial MAG3 uptake is primarily dependent upon tubular secretion rather than GFR. However, later clearance of MAG3 is dependent upon GFR (therefore, decreased excretion is the primary finding). Rarely, the split function will change when MAG3 is used in cases of severe RVHT.
Preliminary data suggest that aspirin renography may be as sensitive as captopril renography for detecting RAS. Considering that, compared with captopril, aspirin reduces renal blood flow and thus tubular tracer delivery in poststenotic kidneys, aspirin renography is expected to be more useful, particularly if tubular tracers are used.39,40,41,42,43
Degree of Confidence
Standard renography with131 I-labeled OIH has low specificity and low sensitivity in the diagnosis of RAS.
For RAS greater than 50%, Tc-MAG3 captopril renography has a sensitivity of 90%, a specificity of 91%, a positive predictive value of 70%, and a negative predictive value of 97%.
Data reported by Imanishi et al suggest that iodine-123 OIH or MAG3 renography is more sensitive for the diagnosis of unilateral RVHT when aspirin is given.41 Although Maini et al found that aspirin renography is superior to captopril renography,39 results from van de Ven et al show that, for the identification of RAS, the usefulness of aspirin renography equals but does not surpass that of captopril renography.40
False Positives/Negatives
With standard131 I-labeled OIH radionuclide renography, false-positive results may occur with all conditions that cause unilateral reduction in blood flow. These conditions include chronic pyelonephritis, renal outlet obstruction, renal vein thrombosis, compression of the renal hilum, perirenal abscess, perirenal hematoma, and ptosis of the kidney.
In patients with RVHT, a captopril renogram may yield false-negative results after the long-term administration of captopril despite adequately maintained blood pressure. Therefore, where possible, ACE inhibitors should be discontinued before captopril renography. Overhydration may lead to a false-negative result, and underhydration may lead to a false-positive result. Bilateral RAS may be difficult to diagnose. In patients with poor renal function, examinations are nondiagnostic. An asymmetric, small kidney with poor function is often unresponsive to a captopril renogram.
Angiography
Findings
Renal artery stenosis/renovascular hypertension. Left, Flush aortogram in a 63-year-old man with hypertension shows marked stenosis of the right renal artery and complete occlusion of the left renal artery. Note the extensive atheroma in the aorta and iliac arteries. Right, nephrogram-phase image shows a significantly smaller left kidney with a faint nephrogram. Some blood supply to the left kidney is retained via collaterals (see image on the left).
Renal artery stenosis/renovascular hypertension. Digital subtraction flush aortogram in a 77-year-old normotensive man shows marked left renal artery stenosis and diffuse aortic atheroma. The patient presented with lower-limb claudication.
Renal artery stenosis/renovascular hypertension. Left, A balloon angioplasty catheter is seen in situ across the left renal artery stenosis in the same patient as in Image 7 in Multimedia. Right, After angioplasty, an excellent anatomic (and functional) result was achieved.
Renal artery stenosis/renovascular hypertension. Digital subtraction flush aortogram in a patient with a right iliac fossa transplanted kidney. Image shows stenosis at the anastomotic site associated with post-stenotic dilatation.
Renal artery stenosis/renovascular hypertension. Digital subtraction flush aortogram in a patient with a left iliac fossa transplanted kidney. Image shows an intrarenal branch stenosis associated with post-stenotic dilatation.
Conventional angiography remains the criterion standard for the detection of RAS, although CTA and MRA are increasingly being used. The severity of the stenosis and the presence of collateral circulation to the kidney may be assessed to determine the hemodynamic significance of RAS. Lesions occluding more than 50% of the diameter of the artery are considered significant. Both the angiographic and the nephrographic phases can be evaluated; the latter may better depict ischemic changes (see Image below and Image 13 in Multimedia).
Renal artery stenosis/renovascular hypertension. Differential diagnosis. Selective right renal angiogram shows standing waves in an intralobar artery. Standing waves in the renal arteries show as multiple serrated indentations that are symmetrically distributed at evenly spaced intervals. These of no pathologic significance and may represent arterial spasm. They may also affect intrarenal branches, as in this case.
Epinephrine may further restrict blood flow to the kidneys and make the collateral circulation more obvious. Generally, flush aortography suffices for mainstem RAS, but if branch stenosis is suspected, selective renal angiography may better define the lesion. Digital subtraction angiography (DSA) does not address the hemodynamic significance of RAS.
RAS caused by AD generally affects the middle and distal renal artery in 79% of the patients, affects a branch renal artery in 4%, or affects a combination of the 2 in 17%. MFP is bilateral in approximately 65% of cases; the left-to-right ratio is 4:1.
Degree of Confidence
Renal angiography remains the criterion standard in the diagnosis of RAS. Angiography is essential when renovascular intervention is contemplated. The angiographic measurement of the size of RAS — an important parameter in assessing the significance of RAS — is inaccurate. Angiography provides only anatomic information; it does not enable the assessment of blood flow through the stenosis.
False Positives/Negatives
On DSA images, artifact from moving structures, such as occurs with peristalsis, may be mistaken for RAS. Standing waves may be confused with RAS.
More on Renal Artery Stenosis/Renovascular Hypertension |
| Overview: Renal Artery Stenosis/Renovascular Hypertension |
 Imaging: Renal Artery Stenosis/Renovascular Hypertension |
| Follow-up: Renal Artery Stenosis/Renovascular Hypertension |
| Multimedia: Renal Artery Stenosis/Renovascular Hypertension |
| References |
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References
Broekhuizen-de Gast HS, Tiel-van Buul MM, Van Beek EJ. Severe hypertension in children with renovascular disease. Clin Nucl Med. Jul 2001;26(7):606-9. [Medline].
Courtel JV, Soto B, Niaudet P, et al. Percutaneous transluminal angioplasty of renal artery stenosis in children. Pediatr Radiol. Jan 1998;28(1):59-63. [Medline].
Estepa R, Gallego N, Orte L, et al. Renovascular hypertension in children. Scand J Urol Nephrol. Oct 2001;35(5):388-92. [Medline].
Sharathkumar AA, Stanley JC. Management of a child with renal artery stenosis and homozygous factor V Leiden mutation. J Pediatr Surg. Jan 2008;43(1):e17-9. [Medline].
Minor RL Jr, Straw SM. Atherosclerotic Renovascular Disease: Prevalence, Natural History, Noninvasiveive Diagnosis and Endovascular Therapy Using Palmaz Stents. J Invasive Cardiol. Sep 1997;9(7):489-499. [Medline].
Weaver FA, Kuehne JP, Papanicolaou G. A recent institutional experience with renovascular hypertension. Am Surg. Mar 1996;62(3):241-5. [Medline].
Textor SC. Renovascular hypertension in 2007: where are we now?. Curr Cardiol Rep. Nov 2007;9(6):453-61. [Medline].
van Helvoort-Postulart D, Dirksen CD, Nelemans PJ, Kroon AA, Kessels AG, de Leeuw PW, et al. Renal artery stenosis: cost-effectiveness of diagnosis and treatment. Radiology. Aug 2007;244(2):505-13. [Medline].
Patel VI, Conrad MF, Kwolek CJ, LaMuraglia GM, Chung TK, Cambria RP. Renal artery revascularization: outcomes stratified by indication for intervention. J Vasc Surg. Jun 2009;49(6):1480-9. [Medline].
Leesar MA, Varma J, Shapira A, Fahsah I, Raza ST, Elghoul Z, et al. Prediction of hypertension improvement after stenting of renal artery stenosis: comparative accuracy of translesional pressure gradients, intravascular ultrasound, and angiography. J Am Coll Cardiol. Jun 23 2009;53(25):2363-71. [Medline].
Jensen G, Annerstedt M, Klingenstierna H, Herlitz H, Aurell M, Hellström M. Survival and quality of life after renal angioplasty: a five-year follow-up study. Scand J Urol Nephrol. 2009;43(3):236-41. [Medline].
Goldblatt H, Lynch J, Hanzal RF, Summerville WW. Studies on experimental hypertension. I The production of persistent elevation of systolic blood pressure by means of renal ischemia. J Exp Med. 1934;59:347-348.
Kasirajan K, O'Hara PJ, Gray BH, Hertzer NR, Clair DG, Greenberg RK, et al. Chronic mesenteric ischemia: open surgery versus percutaneous angioplasty and stenting. J Vasc Surg. Jan 2001;33(1):63-71. [Medline].
BURKLAND CE, GOODWIN WE, LEADBETTER WF. The cure of hypertension by nephrectomy; a ten-year follow-up of a case. Surgery. Jul 1950;28(1):67-70. [Medline].
Leadbetter WF, Burkland CE. Hypertension in unilateral renal disease. J Urol. 1938;39:611-625.
McCormack LJ, Dusten HP, Meaney TF. Selected pathology of the renal artery. Semin Roentgenol. 1967;2:126-138.
Rafalowska J. Genetically determined vascular diseases. Folia Neuropathol. 1999;37(4):210-6. [Medline].
Goncharenko V, Gerlock AJ Jr, Shaff MI, Hollifield JW. Pregression of renal artery fibromuscular dysplasia in 42 patients as seen on angiography. Radiology. 1981;139:45-51.
Kuczera P, Wloszczynska E, Adamczak M, Pencak P, Chudek J, Wiecek A. Frequency of renal artery stenosis and variants of renal vascularization in hypertensive patients: analysis of 1550 angiographies in one centre. J Hum Hypertens. Jun 2009;23(6):396-401. [Medline].
Crowley JJ, Santos RM, Peter RH, Puma JA, Schwab SJ, Phillips HR, et al. Progression of renal artery stenosis in patients undergoing cardiac catheterization. Am Heart J. Nov 1998;136(5):913-8. [Medline].
Holley KE, Hunt JC, Brown AL, Kincaid OW, Sheps SG. Renal artery stenosis. A clinical-pathological study in normotensive and hypertensive patients. Am J Med. 1964;37:124–132.
Gilfeather M, Yoon HC, Siegelman ES, Axel L, Stolpen AH, Shlansky-Goldberg RD, et al. Renal artery stenosis: evaluation with conventional angiography versus gadolinium-enhanced MR angiography. Radiology. Feb 1999;210(2):367-72. [Medline].
Vasbinder GB, Nelemans PJ, Kessels AG, et al. Diagnostic tests for renal artery stenosis in patients suspected of having renovascular hypertension: a meta-analysis. Ann Intern Med. Sep 18 2001;135(6):401-11. [Medline].
Textor SC, Glockner JF, Lerman LO, Misra S, McKusick MA, Riederer SJ, et al. The use of magnetic resonance to evaluate tissue oxygenation in renal artery stenosis. J Am Soc Nephrol. Apr 2008;19(4):780-8. [Medline].
Durand E, Blaufox MD, Britton KE, Carlsen O, Cosgriff P, Fine E, et al. International Scientific Committee of Radionuclides in Nephrourology (ISCORN) consensus on renal transit time measurements. Semin Nucl Med. Jan 2008;38(1):82-102. [Medline].
Lie JT. Pathology of angiodysplasia in Klippel-Trenaunay syndrome. Pathol Res Pract. Nov 1988;183(6):747-55. [Medline].
Beregi JP, Louvegny S, Gautier C, et al. Fibromuscular dysplasia of the renal arteries: comparison of helical CT angiography and arteriography. AJR Am J Roentgenol. Jan 1999;172(1):27-34. [Medline].
Saba L, Sanfilippo R, Montisci R, Conti M, Mallarini G. Accessory renal artery stenosis and hypertension: are these correlated? Evaluation using multidetector-row computed tomographic angiography. Acta Radiol. Apr 2008;49(3):278-84. [Medline].
Drieghe B, Madaric J, Sarno G, Manoharan G, Bartunek J, Heyndrickx GR, et al. Assessment of renal artery stenosis: side-by-side comparison of angiography and duplex ultrasound with pressure gradient measurements. Eur Heart J. Feb 2008;29(4):517-24. [Medline].
Josephs SC. Techniques in interventional radiology: renal CT angiography. Tech Vasc Interv Radiol. Dec 2006;9(4):167-71. [Medline].
Andreoni KA, Weeks SM, Gerber DA, et al. Incidence of donor renal fibromuscular dysplasia: does it justify routine angiography?. Transplantation. Apr 15 2002;73(7):1112-6. [Medline].
Marcos HB, Choyke PL. Magnetic resonance angiography of the kidney. Semin Nephrol. Sep 2000;20(5):450-5. [Medline].
Papachristopoulos G, Bis KG, Shetty AN. Breath-hold 3D MR angiography of the renal vasculature using a contrast- enhanced multiecho gradient-echo technique. Invest Radiol. Dec 1999;34(12):731-8. [Medline].
Stacul F, Gava S, Belgrano M, Cernic S, Pagnan L, Pozzi Mucelli F, et al. Renal artery stenosis: Comparative evaluation of gadolinium-enhanced MRA and DSA. Radiol Med (Torino). May 15 2008;[Medline].
Hoshino Y, Nakamura T, Nakano A, et al. Successful treatment of renovascular hypertension due to fibromuscular dysplasia by intravascular ultrasound-guided atherectomy. Nephron. Jul 2002;91(3):521-5. [Medline].
Majd M, Potter BM, Guzzetta PC, Ruley EJ. Effect of captopril on efficacy of renal scintigraphy in detection of renal artery stenosis. J Nucl Med. 1983;24:23.
Fine EJ. Diuretic renography and angiotensin converting enzyme inhibitor renography. Radiol Clin North Am. Sep 2001;39(5):979-95. [Medline].
Goto A, Kawauchi N. Images in clinical medicine. Captopril-augmented renal scan. N Engl J Med. Feb 8 2001;344(6):430. [Medline].
Maini A, Gambhir S, Singhal M. Aspirin renography in the diagnosis of renovascular hypertension: a comparative study with captopril renography. Nucl Med Commun. Apr 2000;21(4):325-31. [Medline].
van de Ven PJ, de Klerk JM, Mertens IJ, et al. Aspirin renography and captopril renography in the diagnosis of renal artery stenosis. J Nucl Med. Aug 2000;41(8):1337-42. [Medline].
Imanishi M, Yano M, Okumura M, et al. Aspirin renography in diagnosis of unilateral renovascular hypertension. Hypertens Res. Sep 1998;21(3):209-13. [Medline].
Ergun EL, Caglar M, Erdem Y, et al. Tc-99m DTPA acetylsalicylic acid (aspirin) renography in the detection of renovascular hypertension. Clin Nucl Med. Sep 2000;25(9):682-90. [Medline].
Kiratli PO, Caner B, Altun B. Superiority of tc-99m MAG3 to tc-99m DTPA in treating a patient with mild renal artery stenosis. Ann Nucl Med. Feb 2001;15(1):45-8. [Medline].
Birrer M, Do DD, Mahler F, et al. Treatment of renal artery fibromuscular dysplasia with balloon angioplasty: a prospective follow-up study. Eur J Vasc Endovasc Surg. Feb 2002;23(2):146-52. [Medline].
van Jaarsveld BC, Krijnen P, Pieterman H, et al. The effect of balloon angioplasty on hypertension in atherosclerotic renal-artery stenosis. Dutch Renal Artery Stenosis Intervention Cooperative Study Group. N Engl J Med. Apr 6 2000;342(14):1007-14. [Medline].
Wykrzykowska JJ, Williams M, Laham RJ. Stabilization of renal function, improvement in blood pressure control and pulmonary edema symptoms after opening a totally occluded renal artery. J Invasive Cardiol. Jan 2008;20(1):E26-9. [Medline].
Eklöf H, Bergqvist D, Hägg A, Nyman R. Outcome after endovascular revascularization of atherosclerotic renal artery stenosis. Acta Radiol. Apr 2009;50(3):256-64. [Medline].
O''Neill JA Jr. Long-term outcome with surgical treatment of renovascular hypertension. J Pediatr Surg. Jan 1998;33(1):106-11. [Medline].
Porter GA. Contrast associated nephropathy. Am J Cardiol. 1989;64:22E-26E.
Further Reading
Keywords
renal artery stenosis, renovascular hypertension, RAS, RVHT, atheromatous renal artery stenosis, renal artery fibrosing lesions, intimal fibroplasia, medial fibrosis with microaneurysms, subadventitial fibroplasia, fibromuscular hyperplasia, segmental mediolytic arteriopathy, renal ischemia, renin-angiotensin-aldosterone activation, arterial dysplasia, medial fibroplasia, MFP
